Evidence map›Paper›PMID 22776234›Full record

ReviewChinese journal of cancer2013

The genetics and biology of KRAS in lung cancer.

Peter M K Westcott, Minh D To

Abstract readReview
In one paragraph

Review in Chinese journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed.

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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Peter M K WestcottPharmaceutical Sciences and Pharmacogenomics Program, Helen Diller Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94115, USA.
Minh D To

Funding

PHARMACEUTICAL SCIENCES AND PHARMACOGENOMICST32GM007175 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AHITUV, NADAV, KROETZ, DEANNA L · 1985 to 2021
$7.1M
NIGMS NIH HHS T32 GM007175
6 · The paper itself

Abstract

Mutational activation of KRAS is a common oncogenic event in lung cancer and other epithelial cancer types. Efforts to develop therapies that counteract the oncogenic effects of mutant KRAS have been largely unsuccessful, and cancers driven by mutant KRAS remain among the most refractory to available treatments. Studies undertaken over the past decades have produced a wealth of information regarding the clinical relevance of KRAS mutations in lung cancer. Mutant Kras-driven mouse models of cancer, together with cellular and molecular studies, have provided a deeper appreciation for the complex functions of KRAS in tumorigenesis. However, a much more thorough understanding of these complexities is needed before clinically effective therapies targeting mutant KRAS-driven cancers can be achieved.

Indexed as

MutationAnimalsCarcinoma, Non-Small-Cell LungCell Transformation, NeoplasticDisease SusceptibilityGene Knockdown TechniquesGenetic TherapyHumansLung NeoplasmsMiceNeoplasms, ExperimentalProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRNA, Small InterferingSignal TransductionKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRNA, Small Interfering

Identifiers

PMID22776234
PMCPMC3845615

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.